Venous insufficiency is a term used to describe a functional failure of venous valves in a venous system. This functional failure can occur when venous veins distend and the venous valves become incompetent because the outermost edges of the venous veins do not approximate and close as a pair. In general, the venous valves may be prone to failure due to numerous conditions and co-morbidities. Unfortunately, venous insufficiency is often undiagnosed until late clinical manifestations because of its difficulty to detect.
Deep vein thrombosis and pulmonary embolism (hereafter collectively termed “venous thromboembolism”), a progression of venous insufficiency, are significant medical conditions that have high morbidity and mortality. For example, research has estimated that over 200,000 new cases of venous thromboembolism occur annually. Further, venous thromboembolism can occur as a culmination of a series of pathophysiologic events that can manifest in patients of all ages with high risk factors. Some of these high risk factors can include, but are not limited to, any of the following conditions in a patient: antithrombin deficiency, proteins C & S deficiencies, factor V leiden, prothrombin mutation, age greater than 40 years, malignancy, antiphospholipid antibodies, history of venous thromboembolism, prolonged immobilization, “economy class syndrome,” bed rest, pregnancy, oral contraceptives/hormone replacement therapy, ischemic (non-hemorrhagic) stroke, pneumonia and respiratory failure, chronic inflammatory disorder and/or active collagen vascular disorder.
In brief, the pathophysiology of venous thromboembolism is based on pooling of venous blood that forms clots (deep vein thrombosis). These clots lodge within the veins, particularly within deep veins of a patient's extremities, but can also form at other locations in a patient's body. As the length of time of venous stasis increases, i.e., the length of time when blood “pools” or is not propagated under normal physiologic parameters, the elastic veins distend and further render the venous valves incompetent, leading to more pooling and coagulation of blood, also known as clot formation. After clot formation, the clot can then fragment or dislodge from the veins and propagate to a heart of the patient, and then to the clot's final destination, the patient's lung, thereby forming a pulmonary embolism (hereafter “PE”).
The PE physically blocks the gas exchange function of the lung and, if the clot is large enough, the PE can be instantly fatal to the patient. Approximately 70% of patients with fatal PEs are diagnosed only at an autopsy because the PE diagnosis is not usually suspected clinically by doctors. The majority of patients with medium to large PEs die within thirty minutes after the onset of symptoms, thereby preventing timely administration of thrombolytic therapy or surgical intervention. Improved methods of deep vein thrombosis prevention are therefore needed to lower mortality associated with PE.
Current prophylactic treatments for venous thromboembolism can include two treatment options: pharmaceutical and non-pharmaceutical modalities. The pharmaceutical modalities can include anticoagulation therapy, such as the administration of heparin or low molecular weight heparin, warfarin (Coumadin™), etc., which therapies may sometimes have significant bleeding risk because of the reduced viscosity in the patient's blood associated therewith. Thus, these pharmaceutical modalities must be used in a controlled setting. Often pharmaceutical modalities can require that the patient be in a hospital or an outpatient care facility during use and require routine blood monitoring and adjustment in dose for proper anticoagulation. Non-pharmaceutical modalities can include compression hosieries and various pneumatic sequential compression devices (hereafter “SCD” or “SCDs”) and constitute one of the most functional and, likely the least invasive, form of prophylaxis.
Pneumatic SCDs have been used mostly for incompetent vascular circulation of the patient's lower extremities. To date, most therapeutic uses of SCDs occur within an inpatient care setting and use cumbersome pneumatic pumps. These pneumatic SCDs provide for external compression of the lower extremities to mimic a physiologic pumping action of the patient's leg musculature for venous return of blood to the heart and for perpetuating systemic anticoagulant factor release from endothelial cells.
The pneumatic SCDs typically consist of three separate components that must be connected together in order for the SCD to function properly. These components are generally: (1) large, plug-in, motor units, (2) tubing, and (3) compression sleeves or stockings that are typically attached to the lower extremities of the patient. Once the three components are attached and functioning, the pneumatic SCD can render the patient immobile, or virtually immobile, because of the trip and fall hazard associated with ambulating with an anchored motor unit and/or the tubing that attaches all three components. The pneumatic SCD's components only work as a unit when all three components are attached to each other and when the unit is plugged into an electricity source. Thus, when a patient disconnects the sleeve or stocking from the tubing in order to ambulate, the pneumatic SCD is no longer functional.
Inherent problems with all pneumatic SCDs are their size, weight, immobility, and disruptive noise level. Further, most pneumatic SCDs offer only a cuff or sleeve, which is worn on the limb or extremity of a patient, and can restrict the patient's functional motion. Most available pneumatic SCDs do not have battery options, and those that do can be quite cumbersome and make mobile operation nearly impossible for the patient. What is needed is an improvement over the foregoing.